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CHAPTER 2
NERVE AGENTS
Section I. INTRODUCTION
2-1. General
a. Nerve agents are a group of highly toxic
organic esters of phosphoric acid derivatives. These
agents have physiological effects (inhibition of cholinesterase) resembling those of physostigmine and
pyridostigmine. However, they are more potent,
longer-acting, and tend to be irreversible after a time
which varies with the agent.
b. Nerve agents are among the deadliest of
chemical agents and may produce rapid symptoms.
They include the G- and V-agents. Examples of Gagents are Tabun (GA), Sarin (GB), Soman (GD),
and GF. A V-agent is VX. In some countries, “V”
agents are known as “A” agents. (Detailed descriptions of nerve agents are found in FM 3-9.)
c. Nerve agents can be dispersed by artillery shell,
mortar shell, rocket, land mine, missile, aircraft spray,
and aircraft bomb or bomblet.
d. Several related but somewhat less toxic compounds have proven to be useful in medicine and
agriculture, as indicated below. The symptoms and
treatment of poisoning by these compounds are similar
to those of poisoning by nerve agents.
(1) Anticholinesterase agents have been used
in the treatment of abdominal distention, urinary
retention, and glaucoma.
(2) Many of the insecticides currently in use
are organophosphates and are chemically related to
nerve agents. Although beneficial for arthropod
control, their widespread use has caused many accidental poisonings—some fatal. Organophosphate
insecticides may have a slower and longer lasting
effect as compared to CW organophosphates.
2-2. Physical and Chemical Properties
Nerve agents are colorless to light brown liquids.
Some are volatile, while others are relatively nonvolatile at room temperature. Most nerve agents are
essentially odorless; however, some have a faint fruity
odor. In toxic amounts, aqueous solutions of nerve
agents are tasteless. The G-agents tend to be nonpersistent, whereas the V-agents are persistent. However,
thickened nonpersistent agents may present a hazard
for an extended period of time. These agents are
moderately soluble in water with slow hydrolysis; are
highly soluble in lipids; and are rapidly inactivated by
strong alkalies and chlorinating compounds (strong
alkalies and chlorinating compounds are used for
decontaminating equipment; in diluted formulas,
chlorinating compounds are used for patient decontamination).
2-3. Absorption of and Protection Against
Nerve Agents
a. Nerve agents may be absorbed through any
body surface. When dispersed as a spray or aerosol,
droplets can be absorbed through the skin, eyes, and
respiratory tract. When dispersed as a vapor at
expected field concentrations, the vapor is primarily
absorbed through the respiratory tract. If enough
agent is absorbed, local effects are followed by
generalized systemic effects. The rapidity with which
effects occur is directly related to the amount of agent
absorbed in a given period of time. Liquid nerve
agents may be absorbed through the skin, eyes, mouth,
and membranes of the nose. Nerve agents may also
be absorbed through the gastrointestinal tract when
ingested with food or water. Local effects after skin
exposure are localized sweating and/or muscular
twitching. Local effects after vapor or liquid exposure
to the eye include miosis and often conjunctival hyperemia. Local effects of liquid on the mucous
membrane include twitching or contracting of the
underlying muscle and glandular secretions. Absorption of a nerve agent by any route may result in
generalized systemic effects. The respiratory tract
(inhalation) is the most rapid and effective route of
absorption.
b. The protective mask and hood protect the face
and neck, eyes, mouth, and respiratory tract against
nerve agent spray, vapor, and aerosol. Nerve agent
vapor (in expected field concentrations) is absorbed
through the skin very slowly, if at all, so proper
masking may protect against the effects of low vapor
concentrations. To prevent inhaling an incapacitating
or lethal dose, hold your breath and put on your mask
within 9 seconds at the first warning of a nerve agent
presence.
c. Liquid nerve agents penetrate ordinary clothing
rapidly. However, significant absorption through the
skin requires a period of minutes. The effects may be
reduced by quickly removing contaminated clothing
and neutralizing liquid nerve agent on the skin (washed
off, blotted, or wiped away). Prompt decontamination
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of the skin is imperative. Decontamination of nerve
agents on the skin within 1 minute after contamination
is perhaps ten times more effective than it would be if
delayed 5 minutes. A nerve agent on the skin can be
removed effectively by using the M291 Skin Decontaminating Kit or the M258A1 Skin Decontamination
Kit (app D). The M291 Skin Decontaminating Kit is
replacing the M258A1. Upon receipt of the M291,
discontinue using the M258A1 on the skin. Liquid
nerve agent in the eye is absorbed faster than on the
skin and is extremely dangerous; immediately irrigate
the eye with copious amounts of water.
d. The chemical protective overgarment, patient
protective wrap (PPW), impermeable protective
gloves, and overboots protect the skin against nerve
agents in liquid, aerosol, and vapor forms.
2-4. Effects of Nerve Agents
a. Mechanism of Action. The effects of nerve
agents (table 2-1 ) are due to their ability to inhibit
cholinesterase enzymes throughout the body. Since
the normal function of these enzymes is to hydrolyze
acetylcholine wherever it is released, such inhibition
results in the accumulation of excessive concentrations
of acetylcholine at its various sites of action. These
include the endings of the autonomic nerves to the
smooth muscle of the iris, ciliary body, bronchial tree,
gastrointestinal tract, bladder, and blood vessels; to
the salivary glands and secretory glands of the
gastrointestinal tract and respiratory tract; and to the
cardiac muscle and endings of sympathetic nerves to
the sweat glands (fig 2-l). The accumulation of
acetylcholine at these sites results in characteristic
muscarinic signs and symptoms (table 2-1). The
accumulation of acetylcholine at the endings of motor
nerves to voluntary muscles and in some autonomic
ganglia results in nicotinic signs and symptoms (table
2-l). Finally, the accumulation of excessive acetylcholine in the brain and spinal cord results in characteristic CNS symptoms (table 2-1). The inhibition
of cholinesterase enzymes throughout the body by
nerve agents may be irreversible and their effects
prolonged; therefore, treatment should begin promptly
before irreversibility occurs. Until the tissue cholinesterase enzymes are restored to normal activity,
there is a period of increased susceptibility to the
effects of another exposure to any nerve agent. This
period of increased susceptibility occurs during the
enzyme regeneration phase which could last from
weeks to several months, depending on the severity of
the initial exposure. During this period the effects of
repeated exposures are cumulative.
b. Pathology. Aside from the decrease in the
activity of cholinesterase enzymes throughout the body
(which may be analyzed by laboratory methods), no
specific lesions are detectable by ordinary gross
examination. At postmortem examination there is
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usually capillary dilation, hyperemia, and edema of
the lungs; there may be similar changes in the brain
and the remaining organs. Neuropathologic changes
have been reported in animals following severe
intoxication.
c. Effects of Vapor. The lungs and the eyes absorb
nerve agents rapidly. Changes occur in the smooth
muscle of the eye, resulting in miosis (contraction of
the pupil); also in the smooth muscle and secretory
glands of the bronchi, producing bronchial constriction
and excessive secretions in the upper and lower
airways. In high vapor concentrations, the nerve agent
is carried from the lungs throughout the circulatory
system; widespread systemic effects may appear in
less than 1 minute.
(1) Local ocular effects. These effects begin
within seconds or minutes after exposure and before
there is any evidence of systemic absorption. The
earliest ocular effect which follows minimal symptomatic exposure to vapor is miosis. This is an
invariable sign of ocular exposure to enough vapor to
produce symptoms. It is also the last ocular manifestation to disappear. The pupillary constriction may
be different in each eye. Within a few minutes after
the onset of exposure, there also occurs redness of the
eyes due to conjunctival hyperemia and a sensation of
pressure with heaviness in and behind the eyes.
Usually vision is not grossly impaired, although there
may be a slight dimness especially in the peripheral
fields or when in dim or artificial light. Exposure to
a level of a nerve agent vapor slightly above the
minimal symptomatic dose results in miosis; pain in
and behind the eyes attributable to ciliary spasm,
especially on focusing; some difficulty of accommodation; and frontal headache. The pain becomes
worse when the casualty tries to focus the eyes or
looks at a bright light. Some twitching of the eyelids
may occur. Occasionally there is nausea and vomiting
which, in the absence of systemic absorption, may be
due to a reflex initiated by the ocular effects. These
local effects may result in moderate discomfort and
some loss of efficiency, but may not necessarily
produce casualties. Following minimal symptomatic
exposure, the miosis lasts from 24 to 72 hours. After
exposure to at least the minimal symptomatic dose,
miosis is well established within half an hour. Miosis
remains marked during the first day after exposure
and then diminishes gradually over 2 to 3 days after
MODERATE exposure, but may persist for as long
as 14 days after severe exposure. The conjunctival
erythema, eye pain, and headache may last from 2 to
15 days depending on the dose.
(2) Local respiratory effects. Following
minimal exposure, the earliest effects on the
respiratory tract are watery nasal discharge, nasal
hyperemia, sensation of tightness in the chest,
and occasionally, prolonged wheezing expiration
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suggestive of bronchoconstriction or increased
bronchial secretion. The rhinorrhea usually lasts for
several hours after minimal exposure and for about 1
day after more severe exposure. The respiratory
symptoms are usually intermittent for several hours
duration after MILD exposure; they may last for 1 or
2 days after more severe exposure.
(3) Systemic effects.
The sequence of
symptoms varies with the route of exposure. While
respiratory symptoms are generally the first to appear
after inhalation of nerve agent vapor, gastrointestinal
symptoms are usually the first after ingestion.
Following comparable degrees of exposure, respiratory manifestations are most severe after inhalation
and gastrointestinal symptoms may be most severe
after ingestion. Otherwise, the systemic manifestations
are, in general, similar after any exposure to nerve
agent poisoning by any route. If local ocular exposure
has not occurred, the ocular manifestations (including
miosis) initially may be absent. The signs, symptoms,
and their time course following exposure to nerve
agent are given in table 2-2. The systemic effects
may be considered to be nicotinic, muscarinic, or by
any action at receptors within the CNS. The predominance of muscarinic, nicotinic, or CNS effects
will influence the amount of atropine, oxime, or
anticonvulsant which must be given as therapy. These
effects will be considered separately.
(a) Muscarinic effects. The tightness in
the chest is an early local symptom of respiratory
exposure. This symptom progressively increases as
the nerve agent is absorbed into the systemic circulation, whatever the route of exposure. After
MODERATE or severe exposure, excessive bronchial
and upper airway secretions occur and may become
very profuse, causing coughing, airway obstruction,
and respiratory distress. Audible wheezing may
occur, with prolonged expiration and difficulty in
moving air into and out of the lungs, due to the
increased bronchial secretion or to bronchoconstriction, or both. Some pain may occur in the lower
thorax and salivation increases. Bronchial secretion
and salivation may be so profuse that watery secretions
run out of the sides of the mouth. The secretions may
be thick and tenacious. If postural drainage or suction
is not employed, these secretions may add to the
airway obstruction. Laryngeal spasm and collapse of
the hypopharyngeal musculature may also obstruct the
airway. The casualty may gasp for breath, froth at
the mouth, and become cyanotic. If the upper airway
becomes obstructed by secretions, laryngeal spasm,
or hypopharyngeal musculature collapse, or if the
bronchial tree becomes obstructed by secretions or
bronchoconstriction, little ventilation may occur despite respiratory movements. As hypoxemia and
cyanosis increase, the casualty will fall exhausted and
become unconscious. Following inhalation of nerve
agent vapor, the respiratory manifestations predominate over the other muscarinic effects; they are likely
to be most severe. in older casualties and in those with
a history of respiratory disease, particularly bronchial
asthma. However, if the exposure is not so overwhelming as to cause death within a few minutes,
other muscarinic effects appear. These include sweating, anorexia, nausea, and epigastric and substernal
tightness with heartburn and eructation. If absorption
of the nerve agent has been great enough (whether
due to a single large exposure or to repeated smaller
exposures), there may follow abdominal cramps,
increased peristalsis, vomiting, diarrhea, tenesmus,
increased lacrimation, and urinary frequency. Cardiovascular effects are occasional early bradycardia,
transient tachycardia and/or hypertension followed by
hypotension, and cardiac arrhythmias. The casualty
perspires profusely, may have involuntary defecation
and urination, and may go into cardiorespiratory arrest
followed by death.
(b) Nicotinic effects. With the appearance of MODERATE muscarinic systemic effects,
the casualty begins to have increased fatigability and
MILD generalized weakness which is increased by
exertion. This is followed by involuntary muscular
twitching, scattered muscular fasciculations, and
occasional muscle cramps. The skin may be pale due
to vasoconstriction and blood pressure moderately
elevated (transitory) together with tachycardia,
resulting from epinephrine response to excess
acetylcholine. If the exposure has been severe, the
muscarinic cardiovascular symptoms will dominate
and the fascicular twitching (which usually appear first
in the eyelids and in the facial and calf muscles)
becomes generalized. Many rippling movements are
seen under the skin and twitching movements appear
in all parts of the body. This is followed by severe
generalized muscular weakness, including the muscles
of respiration. The respiratory movements become
more labored, shallow, and rapid; then they become
slow and finally intermittent. Later, respiratory
muscle weakness may become profound and contribute
to respiratory depression. Central respiratory depression may be a major cause of respiratory failure.
(c) Central nervous system effects. In
MILD exposures, the systemic manifestations of nerve
agent poisoning usually include tension, anxiety,
jitteriness, restlessness, emotional lability, and
giddiness. There may be insomnia or excessive
dreaming, occasionally with nightmares. If the
exposure is more marked, the following symptoms
may be evident: headache, tremor, drowsiness, difficulty in concentration, memory impairment with slow
recall of recent events, and slowing of reactions. In
some casualties, there is apathy, withdrawal, and
depression. With the appearance of MODERATE
symptoms, abnormalities of the electroencephalogram
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occur, characterized by irregularities in rhythm, variations in potential, and intermittent bursts of abnormally
slow waves of elevated voltage similar to those seen
in patients with epilepsy. These abnormal waves
become more marked after 1 or more minutes of
hyperventilation which, if prolonged, may occasionally precipitate a generalized convulsion. If absorption
of nerve agent has been great enough, the casualty
becomes confused and ataxic. The casualty may have
changes in speech (consisting of slurring, difficulty in
forming words, and multiple repetition of the last
syllable). The casualty may then become comatose,
reflexes may disappear, and respiration may become
Cheyne-Stokes in character. Finally, generalized
convulsions may ensue. With the appearance of severe
CNS symptoms, central respiratory depression will
occur (adding to the respiratory embarrassment that
may already be present) and may progress to respiratory arrest. However, after severe exposure, the
casualty may lose consciousness and promptly convulse without other obvious symptoms. Death is
usually due to respiratory arrest and anoxia. Prompt
initiation of assisted ventilation may prevent death.
Depression of the circulatory centers may also occur,
resulting in a marked reduction in heart rate with a
fall of blood pressure some time before death.
d. Effects of Liquid Nerve Agent.
(1) Local ocular effects. The local ocular
effects are similar to the effects of nerve agent vapor.
If the concentration of the liquid nerve agent contaminating the eye is high, the effects will be instantaneous and marked; and, if the exposure of the two
eyes is unequal, the local manifestations may be
unequal. Hyperemia may occur but there is no
immediate local inflammatory reaction such as may
occur following ocular exposure to more irritating
substances (for example, lewisite).
(2) Local skin effects. Following cutaneous
exposure, there is localized sweating at and near the
site of exposure and localized muscular twitching and
fasciculation. However, these may not be noticed
causing the skin absorption to go undetected until
systemic symptoms begin.
(3) Local gastrointestinal effects. Following
the ingestion of substances containing a nerve agent
(which is essentially tasteless), the initial symptoms
include abdominal cramps, vomiting, and diarrhea.
(4) Systemic effects. The sequence of symptoms varies with the route of exposure. While respiratory symptoms are generally the first to appear
after inhalation of a nerve agent vapor, gastrointestinal symptoms are usually the first after ingestion.
Following comparable degrees of exposure, respiratory manifestations are most severe after inhalation,
and gastrointestinal symptoms may be most severe
after ingestion. Otherwise, the systemic manifestations
are, in general, similar after any exposure to nerve
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agent poisoning by any route. If local ocular exposure
has not occurred, the ocular manifestations (including
miosis) initially may be absent.
e. Time Course of Effects of Nerve Agents.See
table 2-2.
f. Cumulative Effects of Repeated Exposure.
Daily exposure to concentrations of a nerve agent
insufficient to produce symptoms following a single
exposure may result in the onset of symptoms after
several days. Continued daily exposure may be
followed by increasingly severe effects. After symptoms subside, increased susceptibility may persists for
up to 3 months. The degree of exposure required to
produce recurrence of symptoms and the severity of
these symptoms depend on the dose received and the
time interval since the last exposure. Increased susceptibility is not limited to the particular nerve agent
initially absorbed.
g. Cause of Death. In the absence of treatment,
death is caused by anoxia resulting from airway
obstruction, weakness of the muscles of respiration,
and central depression of respiration. Airway obstruction is due to pharyngeal muscular collapse; upper
airway and bronchial secretions; bronchial constriction
and occasionally laryngospasm; and paralysis of the
respiratory muscles. Respiration is shallow, labored,
and rapid, and the casualty may gasp and struggle for
air. Cyanosis increases. Finally, respiration becomes
slow and then ceases resulting in unconsciousness.
The blood pressure (which may have been transitorily
elevated) falls. Cardiac rhythm may become irregular
and death may ensue. The individual may survive
several lethal doses of a nerve agent if assisted
ventilation is initiated via cricothyroidotomy or
endotracheal tube, if airway secretions are cleared by
postural drainage and suction, and if secretions and
bronchial constrictions are diminished by the vigorous
administration of atropine. However, if the exposure
has been overwhelming, amounting to many times the
lethal dose, death may occur as a result of respiratory
arrest and cardiac arrhythmia despite treatment. When
overwhelming doses of the agent are absorbed quickly,
death occurs rapidly without orderly progression of
symptoms.
2-5. Diagnosis of Nerve Agent Poisoning
a. Nerve agent poisoning may be identified from
the characteristic signs and symptoms. If exposure to
vapor has occurred, the pupils will be very small,
usually pinpointed. If exposure has been cutaneous,
or has followed ingestion of a nerve agent in contaminated food or water, the pupils may be normal
or, in the presence of severe systemic symptoms,
slightly to moderately reduced in size. In this event,
the other manifestations of nerve agent poisoning must
be relied on to establish the diagnosis. No other
known chemical agent produces muscular twitching
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and fasciculations, rapidly developing pinpoint pupils,
or the characteristic train of muscarinic, nicotinic,
and CNS manifestations.
b. It is important that all service members know
the following MILD and SEVERE signs and symptoms of nerve agent poisoning. Service members who
have most or all of the symptoms listed below must
IMMEDIATELY receive first aid (self-aid or buddy
aid) (paras 2-11 a and b, respectively).
(1) MILD poisoning (self-aid). Casualties
with MILD symptoms may experience most or all of
the following:
(a) Unexplained runny nose.
(b) Unexplained sudden headache.
(c) Sudden drooling.
(d) Difficulty in seeing (dimness of
vision and miosis).
(e) Tightness in the chest or difficulty
in breathing.
(f) Wheezing and coughing.
(g) Localized sweating and muscular
twitching in the area of the contaminated skin.
(h) Stomach cramps.
(i) Nausea with or without vomiting.
(j) Tachycardia followed by bradycardia.
(2) SEVERE symptoms (buddy aid). Casualties with SEVERE symptoms may experience most
or all of the MILD symptoms, plus most or all of the
following:
(a) Strange or confused behavior.
(b) Increased wheezing and increased
dyspnea (difficulty in breathing).
(c) Severely pinpointed pupils.
(d) Red eyes with tearing.
(e) Vomiting.
(f) Severe muscular twitching and
general weakness.
(g) Involuntary urination and defecation.
(h) Convulsions.
(i) Unconsciousness.
(j) Respiratory failure.
(k) Bradycardia.
Casualties with severe symptoms WILL NOT be able
to treat themselves and MUST RECEIVE prompt
buddy aid (para 2-11 b), CLS aid (paras 2-9 e and
2-12 c), and prompt follow-on medical treatment (paras
2-15 and 2-16) if they are to survive.
c. Casualties with MODERATE poisoning will
experience an increase in the severity of most or all of
the MILD symptoms. Especially prominent will be
fatigue, weakness, and muscle fasciculations. The
progress of symptoms from MILD to MODERATE
indicates either inadequate treatment or continuing
exposure to the agent.
Section II. PREVENTION AND TREATMENT OF NERVE AGENT POISONING
2-6. Essential Elements of Prevention and
Treatment
The essential prevention and treatment elements of
nerve agent poisoning are—
a. Donning the protective mask and hood at the
first indication of a nerve agent attack.
b. Administering the MARK I (para 2-11) as soon
as any signs or symptoms are noted.
c. Administering the CANA to MODERATE to
severely poisoned casualties (para 2-12).
NOTE
The U.S. Navy does not use the MARK I.
Instead, the Navy issues three atropine and
three pralidoxime chloride (2 PAM C1)
auto injectors per person.
d. Removing or neutralizing any liquid contamination immediately.
e. Removing airway secretions if they are obstructing the airway. Airway suction may be needed.
f. Establishing a patent airway (for example, with
a cricothyroidotomy or endotracheal tube) and administering assisted ventilation, if required. Oxygen is
desired, if available.
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2-7. Prevention of Poisoning
a. The respiratory tract absorbs nerve agent vapor
very rapidly. The protective mask must be put on
IMMEDIATELY when it is suspected that nerve
agent vapor is present in the air. Hold the breath until
the mask is on, cleared, and checked. If the nerve
agent concentration in the air is high, a few breaths
may result in the inhalation of enough nerve agent to
be incapacitating or even lethal. When the concentration in the air is low, a longer exposure may
precede the onset of symptoms and the detection of
nerve agent poisoning. Since the effects of a nerve
agent are progressive and cumulative, the prevention
of further absorption is urgent once symptoms have
begun. Protective masks should be worn until the
“all clear” signal is given.
b. DO NOT give nerve agent antidotes for preventive purposes BEFORE contemplated exposure to
a nerve agent. To do so may enhance respiratory
absorption of nerve agents by inhibiting bronchoconstriction and bronchial secretion. Atropine will
degrade performance when taken in doses of more
than 2 milligram (mg) without nerve agent exposure,
especially when maximal visual acuity is required.
Also, atropine will degrade an individual’s ability to
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perform duties in a hot environment. Atropine is
rapidly used up in the treatment of nerve agent
poisoning. A person incapacitated by nerve agent
poisoning will likely remain incapacitated since
atropine will not reverse all the signs and symptoms
of poisoning, even in large doses.
c. Nerve agents (liquid or vapor) can poison food
and water. For details on management and decontamination of food and water, see FM 8-10-7.
2-8. Effects of Nerve Agent Antidotes
a. General.
(1) Atropine. Atropine sulfate remains an
essential drug in the treatment of nerve agent poisoning. It acts by blocking the effects of acetylcholine
at muscarinic receptors and produces relief from many
of the symptoms previously listed. If given in large
doses, some therapeutic effects are also produced
within the CNS although atropine does not readily
penetrate the blood-brain barrier as does diazepam
(para 2-8 a (3)), and central muscarinic receptors are
thought not to be identical with those in the periphery.
It is thought to counteract the respiratory depression
in the medulla oblongata. Used alone, it has little
influence on the mortality rate in the potentially fatal
apneic cases for which assisted ventilation is many
times more effective. However, the combination of
adequate atropinization plus assisted ventilation is
several times more effective in saving lives than
assisted ventilation alone.
(2) 2 PM Cl. 2 PAM Cl is an oxime which
increases the effectiveness of drug therapy in poisoning by some—but not all—cholinesterase inhibitors.
Unlike atropine, 2 PAM Cl acts by blocking the nerve
agent inhibition of cholinesterase and/or reactivating
the inhibited acetylcholinesterase clinically at muscarinic sites. Thus 2 PAM Cl relieves the skeletal
neuromuscular block, as well as reactivating the
acetylcholinesterase clinically at muscarinic sites. The
role of 2 PAM Cl is to block and reverse the bonding
of the nerve agent to the acetylcholinesterase. Oximes
must be given early in the poisoning; after a short
period of time (different for each type of nerve agent),
they may no longer be effective.
NOTE
2 PAM Cl varies in its effectiveness against
nerve agents. It is least effective against
GD.
(3) Diazepam. Diazepam readily crosses the
blood-brain barrier to block the effects of acetylcholine
on the CNS, in contrast to the partial protection of
atropine at best. Diazepam antagonizes the convulsive
action of nerve agents. The addition of diazepam to
the basic antidotes prevents or ameliorates convulsions
in MODERATE to severe nerve agent poisoning.
b. Rate of Absorption.
(1) Atropine. A 2-mg intramuscular (IM)
injection will reach peak effectiveness in 3 to 10
minutes, then blood concentrations will decline. If
the system is unchallenged by a nerve agent, a 2-mg
IM injection will cause atropine effects for several
hours. In the presence of a nerve agent challenge, the
effectiveness of atropine is markedly reduced and the
duration of the agent is significantly shortened. More
frequent doses of atropine will be required to achieve
and maintain atropinization.
(2) 2 PAM Cl. Depending on the degree of
intoxication, a 600-mg IM will be effective in 6 to 8
minutes and will maintain peak effectiveness for
1 hour or more. If the system is unchallenged by a
nerve agent, a 600-mg IM will remain in the circulatory system for several hours without apparent
effect.
(3) Diazepam. A 10-mg IM injection in the
thigh ordinarily produces significant plasma levels in
10 minutes; peak plasma concentrations are obtained
in about 1 hour. The concentrations will then decline
over a prolonged period. Rapid administration of
diazepam by IM autoinjector after nerve agent exposure may more effectively prevent or ameliorate
convulsions. SEVERE nerve agent toxicity may
require multiple 10-mg doses given at about 10 minute
intervals for a maximum of three (3) injections (a total
of 30 mg diazepam) to control convulsions.
c. Symptoms Produced by the Antidotes.
(1) Atropine.
(a) The administration of a single dose
of 2 mg (one autoinjector) of atropine to an individual
who has absorbed minimal or no nerve agent produces
MILD symptoms, including dryness of the skin,
mouth, and throat, with slight difficulty in swallowing.
The individual may have a feeling of warmth, slight
flushing, rapid pulse, some hesitancy of urination,
and an occasional desire to belch. The pupils may be
slightly dilated but react to light. In some individuals,
there may be MILD drowsiness and slowness of
memory and ability to recall. Recipients of atropine
may have the feeling that their movements are slow
and their near vision is blurred. Some individuals
may be mildly relaxed. These symptoms should not
interfere with ordinary activity, except in the occasional individual who proves to be unusually reactive
to the “sensation” effects of atropine (particularly the
feeling of drowsiness). However, mental reaction
may be slightly slowed down (for this reason, aviators
must not fly an aircraft after taking atropine until
cleared by the flight surgeon). If the administration
of 2 mg of atropine is repeated within an hour without nerve agent challenge, the symptoms become
MODERATE. In most of these individuals, there
will be some CNS symptoms (such as drowsiness,
fatigue, slowness of memory and ability to recall, the
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feeling that body movements are slow, and blurred
near vision); but they can continue ordinary activity
with some loss of efficiency. Near vision may be
impaired for as long as 24 hours. After repeated
injections of atropine, heat-stressed individuals will
become casualties ((b) below). A third 2-mg dose of
atropine (again without nerve agent challenge) administered within an hour will result in severe symptoms
which will not permit ordinary activity—in fact, most
individuals will be incapacitated. SEVERE incapacitating symptoms of overatropinization (nerve agent
antidote poisoning) are a very dry mouth; swelling of
the tongue and oral mucous membranes; difficulty in
swallowing; thirst; hoarseness; dry and flushed skin;
dilated pupils; blurred near vision; tachycardia (rapid
pulse); urinary retention (in older individuals); constipation; slowing of mental and physical activity;
restlessness; headache; disorientation; hallucinations;
depression; increased drowsiness; extreme fatigue;
rapid respiratory panting; and respiratory distress.
Abnormal behavior may require restraint. The effects
of atropine without nerve agent challenge are fairly
prolonged, lasting 3 to 5 hours after one or two
injections and 12 to 24 hours after marked overatropinization. Overatropinization may be incapacitating but presents little danger to life in a temperate
environment for the nonheat-stressed individual. A
single dose of 10 mg of atropine has been administered
intravenously to normal young adults without endangering life—even in the absence of any prior
absorption of a nerve agent—although it has produced
very marked signs of overdose.
NOTE
While an unchallenged dose of atropine
may allow individuals to continue normal
duties, they must be closely monitored for
possible heat injury. This is especially
important when at MOPP 4 and the individuals’ ability to perspire is reduced due
to atropine.
(b) In hot, desert, or tropical environments or in heat-stressed individuals, doses of atropine
tolerated well in temperate climates may be seriously
incapacitating by interference with the sweating
mechanism. This can sharply reduce the combat
effectiveness of troops who have suffered little or no
exposure to a nerve agent. In hot climates or in heatstressed individuals, one dose (2 mg) of atropine can
reduce efficiency. Two doses (4 mg) will sharply
reduce combat efficiency, and 6 mg will incapacitate
troops for several hours. In hot, humid climates,
individuals who have inadvertently taken an overdose
of atropine and are exhibiting signs of atropine
intoxication should have their activity restricted. In
addition, these casualties must be kept as cool as
2-10
possible for 6 to 8 hours after injection to avoid serious
incapacitation. Usually, the casualties will recover
fully in 24 hours or less from a significant overdose
of atropine.
(c) Experience in chemical operations
has shown that when troops become alarmed, some
believe they have been exposed to more chemical
agents than they actually have been. Hence, it is
important that service members NOT give themselves
more than one atropine injection (2 mg). Casualties
who are able to ambulate and know who they are and
where they are WILL NOT need any more atropine
injections. If the symptoms do recur additional
atropine, up to two more injections for a total of three
(3), can be administered to these casualties. A service
member must consult with a buddy to determine if he
or she needs additional injections of atropine. If an
individual’s heart rate is above 90, breathing appears
normal, bronchial secretions have diminished, and the
skin is dry, the individual does not need anymore
atropine at this time. Additional atropine is given by
a buddy since casualties requiring more will be unable
to administer additional injections to themselves. The
additional administration of atropine to a service
member with only MILD symptoms must be approached cautiously with at least 10 to 15 minutes
elapsing between successive injections. If the signs of
nerve agent poisoning (para 2-5) disappear, or if signs
of atropinization, such as a heart rate above 90,
diminished bronchial secretions, and dry skin, appear
during one of these 10- to 15-minute periods, no
further injections should be administered. These
casualties should remain under observation without
further injections of atropine unless signs of nerve
agent intoxication reappear.
NOTE
Although one means of determining the
casualty’s need for additional atropine is
the heart rate, assessing his or her respiratory effort is important in the evaluation.
Labored breathing, including coughing,
noisy breathing, wheezing, and gasping for
air, indicates the need for administering
additional atropine. When the heart rate is
not obtainable, the need for additional
atropine may be based on the degree of
respiratory impairment. When adequate
atropine has been given, labored breathing
efforts will be relieved. This assessment
must be performed without compromising
the protective posture of MOPP.
(d) Patients with severe symptoms due
to systemic absorption of a nerve agent have increased
tolerance for atropine. Multiple doses maybe required
before signs of atropinization appear, such as heart
FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11
rate above 90, diminished bronchial secretions, and
dry skin. Large doses are required to ameliorate the
muscarinic effects of nerve agent poisoning. The
absence of increased tolerance for atropine indicates
that nerve agent poisoning probably is not present or
is MILD. In the presence of severe nerve agent
poisoning, as much as 50 mg of atropine may be
required for treatment in a 24-hour period. More
than three injections of atropine will be administered
only by the CLS or medical personnel.
(2) 2 PAM Cl. MILD visual changes maybe
a side effect of 2 PAM Cl. After the administration
of three injections of 2 PAM Cl, generally no further
oxime benefit is attained by additional injections of
2 PAM Cl.
(3) Diazepam. The administration of a single
dose of 10 mg (one autoinjector of CANA) to an
individual who has absorbed minimal or no nerve
agent produces significant performance decrements for
about 2 to 5 hours. The individual will have impaired
vision and decision-making functions over this time
period. Overall alertness may be impaired. There
could also be breathing difficulty. For this reason,
casualties should be lying on their side until they are
alert again. There may be transient irritation, as well
as pain, at the injection sites.
Section III. SELF-AID, BUDDY AID, COMBAT LIFESAVER PROCEDURES,
AND COMBAT MEDIC/CORPSMAN TREATMENT
2-9. Principles of Self-Aid and Buddy Aid
a. The protective mask and hood must be put on
IMMEDIATELY at the first signs of a chemical
attack. (The protective overgarment should have
already been put on prior to the use of chemicals on
the battlefield.) Stop breathing, put on your mask,
clear and seal the mask, and resume breathing. Secure
the mask hood. The mask and protective clothing are
worn continually until the “all clear” signal is given.
b. IMMEDIATELY mask any casualty that does
not have a mask on if the atmosphere is still contaminated.
c. The appearance of nerve agent poisoning
symptoms calls for the immediate IM injection of the
nerve agent antidote (paras 2-11 and 2-12). Since
inhalation will be the most common route of exposure,
the most likely initial symptom will be rhinorrhea
(runny nose), then miosis (dim vision), followed by a
feeling of tightness or constriction in the chest. After
ocular (eyes) splash, there will be immediate miosis.
After cutaneous (skin) splash, the initial systemic
symptoms may be localized sweating and localized
muscular twitching, followed by nausea and abdominal
cramps. After ingestion, the first symptoms are likely
to be nausea and vomiting. In any case, use the nerve
agent antidotes as directed (paras 2-11 and 2- 12).
d. Promptly remove any liquid nerve agent on the
skin, on the clothing, or in the eyes.
(1) If a liquid nerve agent gets on the skin,
decontamination must be accomplished within 1 minute (see app D). Then continue the mission. Examine
the contaminated area occasionally for local sweating
and muscular twitching. If these occur, the nerve agent
antidote should be administered. Combat duties should
be continued, as systemic symptoms of nerve agent
poisoning may not occur or may be MILD if the
decontamination was done immediately and successfully.
(2) If a drop or splash of liquid nerve agent
gets into the eye, instant action is necessary to avoid
serious effects. Irrigate the eye immediately with
water as described in appendix D. During the next
minute, the pupil of the contaminated eye should be
observed by a buddy. If the pupil rapidly gets smaller,
a nerve agent antidote should be administered. If the
pupil does not get smaller, the ocular contamination
was not caused by a nerve agent and atropine is not
needed.
e. If good relief is obtained from one set of MARK
I injections and breathing is normal, carry on with
combat duties. Dryness of the mouth is a good sign—
it means enough atropine has been taken to overcome
the dangerous effects of the nerve agent. If symptoms
of the nerve agent are not relieved, the service member
should be administered two more sets of the MARK I
injections plus one injection of CANA by a buddy, in
accordance with the provisions of paragraph 2-11. If
symptoms still persist and the pulse (heart rate) drops
below 90 per minute, bronchial secretions persist, or
the skin remains moist, then the service member can
be administered additional atropine injections by the
CLS or medical personnel (who carry additional
atropine for the treatment of nerve agent casualties) to
maintain adequate atropinization. The CLS and combat medic/corpsman also carry extra CANA for administration to nerve agent casualties (para 2-12). The
CLS or combat medic/corpsman can administer
additional CANA up to a maximum of three before
evacuating the casualty. Evacuate the service member
to a field MTF as soon as the combat situation permits.
f. Atropine and 2 PAM Cl by injection do not
relieve the local effects of nerve agent vapor on the
eyes. Although the eyes may hurt and there may be
difficulty in focusing and a headache, the service
members should carry on with their duties to the best
of their ability. These symptoms are annoying but not
dangerous.
2-11
FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11
g. Exposure to high concentrations of a nerve
agent may bring on incoordination, mental confusion,
and/or collapse so rapidly that the casualty cannot
perform self-aid. If this happens, the nearest able
service member must render buddy aid.
h. SEVERE nerve agent exposure may rapidly
cause unconsciousness, muscular paralysis, and the
cessation of breathing. When this occurs, antidote
alone will not save life. IMMEDIATELY after a
buddy administers three sets of the MARK I and
CANA, assisted ventilation must be started by medical
personnel, if a resuscitation device is available.
Assisted ventilation should be continued until normal
breathing is restored.
2-10. The Nerve Agent Antidote Kit, MARK I
The Nerve Agent Antidote Kit, MARK I (fig E-1), is
an antidote used by the Army and the Air Force in the
treatment of nerve agent poisoning.
a. Description. The MARK I kit consists of four
separate components: the atropine autoinjector, the
2 PAM Cl autoinjector, the plastic clip, and the foam
carrying case.
(1) The atropine autoinjector consist of a hard
plastic tube containing 2 mg (0.7 milliliter (ml)) of
atropine in solution. It has a pressure activated coiled
spring mechanism which triggers the needle for
injection of the antidote solution. The container is
white plastic with yellow lettering on green
identification and directions labels. The safety cap
is yellow plastic attached to the clip at the rear of the
container. The needle end is a green plastic cap
which, when pressure is applied, activates the spring
mechanism.
(2) The 2 PAM Cl autoinjector is a hard
plastic tube which dispenses 600 mg/2 ml of 2 PAM
Cl (300 mg/ml) solution when activated. It has a
pressure activated coiled spring mechanism identical
to that in the atropine autoinjector. The container is
clear plastic with black lettering on a brown identification label. Directions are in black lettering on a
white background. The safety cap is gray plastic
attached to the clip at the rear of the container. The
needle end is black plastic.
(3) The clip is made of clear hard plastic
constructed to hold the pair of autoinjectors together
while attached to their safety caps. The safety caps
are held flush to the bottom of the plastic clip by a
movable metal retaining flange. The clip container
recesses are labeled with black numbers: “1” for the
atropine and “2” for the 2 PAM Cl autoinjector.
(4) The foam envelope is a charcoal gray
form-fitting case with pressed seams and is designed
to carry both autoinjectors. The envelope is used for
shipping purposes only and is removed by service
members prior to putting the MARK I kits in their
mask carrier.
2-12
b. Issue to Service Members. In the U.S. Army
and the U.S. Air Force, each person is authorized to
carry three sets of the MARK I kit for the treatment
of nerve agent poisoning. The U.S. Navy, however,
does not use the MARK I but, rather, its antidote
components are issued as three atropine and three 2
PAM Cl autoinjectors per person.
c. Protection Against Freezing. The atropine and
the 2 PAM Cl solutions freeze at about 30°F (1°C).
Therefore, when the temperature is below freezing,
the MARK I injectors should be protected against
freezing. Autoinjectors issued to the individual service
member are normally carried in the protective mask
carrier. During cold weather when the temperature is
below freezing, the injectors should be carried in an
inside pocket close to the body. (Should the MARK I
injectors become frozen, they can be thawed and
used. )
2-11. Principles in the Use of the Nerve
Agent Antidote Kit, MARK I
The following are principles to be followed in the
administration of the MARK I (fig E-1).
a. Self-Aid. If you experience most or all of the
MILD symptoms of nerve agent poisoning (para 2-5),
you should IMMEDIATELY hold your breath (DO
NOT INHALE) and put on your protective mask.
Then administer one set of MARK I injections into
your lateral thigh muscle (or buttocks). (Self-aid
procedure for administering the autoinjectors is found
in app E.)
(1) Wait 10 to 15 minutes after giving yourself the first set of injections since it takes that long
for the antidote to take effect. If you are able to
ambulate, know who you are, and where you are, you
WILL NOT need a second set of MARK I injections.
WARNING
Giving yourself a second set of injections
may create a nerve agent antidote overdose, which could result in incapacitation.
(2) If symptoms of nerve agent poisoning are
not relieved after administering one set of MARK I
injections, seek someone else to check your symptoms.
A buddy must administer the second and third sets of
injections, if needed.
b. Buddy Aid. If you encounter a service member
suffering from SEVERE signs of nerve agent poisoning (para 2-5), render the following aid:
(1) Mask the casualty, if necessary. Do not
fasten the hood.
(2) Administer, in rapid succession, three sets
of the MARK I.
Follow administration procedures outlined in appendix E.
FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11
NOTE
Use the casualty’s own antidote autoinjectors when providing aid. Do not use
your injectors on a casualty. If you do,
you may not have any antidote available
when needed for self-aid.
(1) Mask the casualty, if necessary. Do not
fasten the hood.
(2) Administer the CANA with the third
MARK I to prevent convulsions. DO NOT administer
more than one CANA. Follow administration procedures outlined in appendix E.
c. Combat Lifesaver. The CLS must check to
verify if the individual has received three sets of the
MARK I. If not, the CLS performs first aid as
described for buddy aid above. If the individual has
received the initial three sets of MARK I, then the
CLS may administer additional atropine injections at
approximately 15 minute intervals until atropinization
is achieved (that is a heart rate above 90 beats per
minute; reduced bronchial secretions; and reduced
salivation). Administer additional atropine at intervals of 30 minutes to 4 hours to maintain atropinization or until the casualty is placed under the care of
medical personnel. Check the heart rate by lifting the
casualty’s mask hood and feeling for a pulse at the
carotid artery. Request medical assistance as soon as
the tactical situation permits.
d. Combat Medic/Corpsman. A casualty has received three sets of MARK I; however, atropinization
has not been achieved. Administer additional atropine
at approximately 15 minute intervals until atropinization is achieved (that is a heart rate above 90
beats per minute; reduced bronchial secretions and
reduced salivation). Administer additional atropine
at intervals of 30 minutes to 4 hours to maintain
atropinization or until the casualty is evacuated to an
MTF. Check the heart rate by lifting the casualty’s
mask hood and feeling for a pulse at the carotid artery.
Provide assisted ventilation for severely poisoned
casualties, if equipment is available. Monitor the
patient for development of heat stress.
NOTE
DO NOT use your own CANA on the
casualty. You may not have any antidote
for your own treatment, if needed.
2-12. Principles in the Use of Convulsant
Antidote for Nerve Agents
The following are principles to be followed in the
administration of CANA (fig E-1).
a. Self-Aid. The CANA is NOT for use as selfaid. If you know who you are, where you are, and
what you are doing, you do not need CANA. If
symptoms do not subside after self-administering one
MARK I, seek assistance from a buddy.
b. Buddy Aid. In addition to administering the
MARK I antidotes for nerve agents as buddy aid, also
administer the CANA.
c. Combat Lifesaver and Medic/Corpsman. The
CLS or medic/corpsman should administer additional
CANA to casualties suffering convulsions. Administer
a second, and if needed, a third CANA at 5 to 10
minute intervals for a maximum of three injections
(30 mg diazepam). Follow the steps and procedures
described in buddy aid for administering the CANA.
DO NOT give more than two additional injections for
a total of three (one buddy aid plus two by CLS or
medic/corpsman).
2-13. Effects of Atropine
The effect of atropine administration on MILD and
MODERATE cases of nerve agent poisoning may
help confirm the diagnosis. Atropine injection
alleviates most of the muscarinic manifestations. It
has little effect on the CNS symptoms and no effect
on the nicotinic symptoms. If the casualty has
absorbed little or no nerve agent, the administration
of a single dose of 2 mg of atropine produces
symptoms of mild atropinization (tachycardia, dry
mouth) in most individuals and repetition of this dose
within 1 or 2 hours produces MODERATE symptoms
of atropinization in almost all individuals. In contrast,
a casualty with MODERATE symptoms of nerve
agent poisoning will not develop symptoms of atropinization after administration of 2 mg of atropine. A
casualty with severe symptoms of nerve agent poisoning may tolerate—indeed may require—considerably
more than 4 mg of atropine (as much as 50 mg in 24
hours).
2-14. Effects of Convulsant Antidote for
Nerve Agents
Diazepam (CANA) is intended to prevent or
ameliorate convulsions in MODERATE to severe
nerve agent poisoning. A casualty with severe nerve
agent poisoning may require multiple doses of CANA
(30 mg or more).
2-13
FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11
Section IV. TREATMENT IN THE FIELD
(MEDICAL TREATMENT FACILITY)
2-15. Administration of the Nerve Agent
Antidotes
Upon arrival at the MTF a casualty is still presenting
signs/symptoms of nerve agent poisoning (para 2-5).
The casualty has received self-aid, buddy aid, CLS
care, or treatment by the combat medic/corpsman, or
other medical personnel in the field before and during
evacuation. Additional injections of the nerve agent
antidote(s) must be administered at the field MTF.
a. Atropine. Atropinization should have been
achieved before the casualty is evacuated to an MTF;
if not, then atropine is administered as follows:
(1) MILD symptoms should be treated by
administering 2 mg of the atropine every 15 minutes
until signs of atropinization (dry mouth and skin, with
cleared pulmonary secretions) are achieved. Maintain
atropinization until muscarinic signs disappear.
(2) MODERATE symptoms should be
treated by administering 2 mg of the atropine every
10 to 15 minutes until atropinization is achieved.
Maintain atropinization by injecting 2 mg of atropine
as often and long as needed.
(3) SEVERE symptoms should be treated by
administering 2 mg of atropine as frequently as
required until atropinization is achieved. Maintain
atropinization by injecting 2 mg of atropine every 10
to 30 minutes as long as needed.
NOTE
Smoking should be prohibited until the
symptoms of nerve agent poisoning have
subsided.
b. 2 PAM Cl. Specifically as an adjunct to
atropine, 2 PAM Cl may be used to increase the
effectiveness of therapy in poisoning by some, but not
all nerve agents. An important facet of the activity of
2 PAM Cl in such therapy is the reduced duration of
required assisted ventilation.
(1) MILD symptoms should have been treated
by administering at least one 600-mg IM injection of
2 PAM Cl.
(2) MODERATE symptoms should have
been treated by administering one or more 600-mg
IM injections of 2 PAM Cl.
(3) SEVERE symptoms should have been
treated by administering three 600-mg IM injections
of 2 PAM Cl. Repeat the dose at least every hour if
respiration has not improved. Generally, no increased
oxime benefit is obtained after three injections of 2
PAM Cl.
c. Diazepam. Diazepam is used specifically as a
prevention of or treatment for convulsions in nerve
2-14
agent poisoned casualties. If brain damage is to be
prevented in MODERATE to severe nerve agent
poisoned casualties, CANA must be administered
early.
Seizures should be anticipated in all
MODERATE to severe cases and treated with the
CANA and repeated as necessary.
2-16. Administration of Follow-on Medical
Treatment
The following medical treatment may also be administered in a CPS or a clean (uncontaminated)
environment, depending on the patient’s needs. Modifications of these procedures may be used in a contaminated environment although an increase in
exposure will occur. The alternative of not performing
these procedures is death of the patient.
a. Administration of Additional Atropine. For
patients who are in severe respiratory distress or are
convulsing, all three sets of their MARK I autoinjectors should have been given. (Convulsions are
treated with diazepam, as described in c below.) If
relief does not occur and bronchial secretions and
salivation do not decrease, administer additional
atropine as often as needed. In severe nerve agent
poisoning, the effect of each 2-mg atropine injection
may be transient, lasting only 5 to 15 minutes. Therefore, these patients must be closely observed and
atropine repeated at intervals that relieve (or counteract) the muscarinic effects of the nerve agent and
maintain mild atropinization for as long as necessary.
b. Management of Bronchial Secretions and Salivation. Patients having excessive airway secretions
and salivation (an indication for additional atropine)
should be lying on their side, with the foot of the litter
or bed elevated, if possible, to promote drainage. If
airway obstruction is occurring, the collar should be
loosened, the tongue pulled out, and the saliva and
mucus cleared periodically from the mouth and
pharynx by suction. Then an oropharyngeal airway
may be inserted and suction carried out intermittently,
as needed (through and around the airway). If, despite
concentrated efforts to carry out assisted ventilation,
the upper airway remains obstructed and adequate
exchange of air does not occur, insert an endotracheal
tube. High airway resistance because of bronchial
constrictions and secretions may be decreased with
the administration of additional atropine.
c. Management of Convulsions. Severely poisoned casualties that develop convulsions usually
progress rapidly to unconsciousness and generalized
muscular weakness or flaccid paralysis, at which point
external evidences of convulsions cease. Seizures
should be anticipated in all MODERATE to severe
FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11
cases and expectantly treated with CANA/diazepam
and repeated as necessary. Seizing is a prominent
feature of nerve agent poisoning, especially GD.
Administer CANA until seizures are controlled.
d. Treatment of Ocular Symptoms. Ocular
symptoms produced by local absorption of a nerve
agent do not respond to the systemic administration of
atropine. However, minimal pain relief may be
obtained by the local instillation of atropine sulfate
ophthalmic ointment (1 percent), repeated as needed
at intervals of several hours for 1 to 3 days. If local
ocular effects of a nerve agent are present, the size of
the pupils cannot be used as an indicator of the
systemic effects of the nerve agent or the atropine.
e. Gastric Lavage. If water or food contaminated
with a nerve agent has been ingested, colicky abdominal pains, substernal tightness, increased salivation,
and perhaps nausea and vomiting will occur 1/2 hour
or later. If ingestion is known to have occurred, early
gastric lavage with water should be done.
f. Removal of Liquid Nerve Agent. Any liquid
nerve agent on the skin or in the eyes should be
removed immediately.
g. Assisted Ventilation. If respiration is severely
impaired or if it ceases after administration of atropine,
cyanosis will ensue and death will occur within
minutes unless immediate effective assisted ventilation
is begun and maintained until spontaneous respiration
is resumed. Far forward in the field, a cricothyroidotomy is the most practical means of providing an
airway for assisted ventilation, using a hand-powered
ventilator equipped with an NBC filter. When a
casualty reaches an MTF where oxygen and a positive
pressure ventilator is available, these should be
employed continuously until adequate spontaneous
respiration is resumed. An endotracheal tube will
most likely be required.
NOTE
Treatment outlined in paragraphs 2-15 and
2-16 is based on the U.S. Army doctrine
on the use of the MARK I and CANA (diazepam). These procedures do not address
the uniqueness of other environments (such
as the threat in naval operations) where
alternatives may be more constrained,
requiring modification in the procedures.
Procedures to address these variations
should be issued by the services concerned
in accordance with their specific needs.
Section V. NERVE AGENT PYRIDOSTIGMINE PRETREATMENT
2-17. Purpose
a. This section prescribes the use of nerve agent
pyridostigmine pretreatment as an adjunct to the
MARK I. Studies in many different types of animals
indicate that when pyridostigmine is used in conjunction with the MARK I (para 2-10 and app E), the
survivability of nerve agent poisoned casualties may
be enhanced. Also covered in this section are the
individual, unit, and command responsibilities for the
pretreatment regimen.
b. Animal data suggest that any potential benefits
that may be derived from use of this pretreatment
regimen will be realized only in nerve agent poisoned
casualties who have been treated with the Mark I at
the time of nerve agent exposure, and who have taken
their pretreatment medication within 8 hours prior to
nerve agent exposure.
c. Minimal detrimental effects are expected at the
recommended dosages. Adverse effects and contraindications are described in paragraph 2-22 below.
is used. The NAPP consists of a blister pack containing 21 tablets. Each tablet consists of 30-mg
pyridostigmine bromide. Each blister pack (NAPP)
contains enough tablets for 7 days (1 taken every 8
hours).
2-18. The Nerve Agent Pyridostigmine
Pretreatment Tablet Set
a. The Nerve Agent Pyridostigmine Pretreatment
(NAPP) Tablet Set (fig 2-2) contains the pretreatment
medication to be taken within 8 hours prior to
exposure to nerve agents at which time the MARK I
2-15
FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11
b. Service members are initially issued one NAPP
when the chemical protective ensemble is expected to
be opened for use. They are responsible for carrying
the NAPP and safeguarding it against loss. Service
members will secure the blister pack in the sleeve or
breast pocket of the chemical protective ensemble (or
in another part of the ensemble, as directed by local
standing operating procedure (SOP)).
NOTE
In conjunction with the NAPP, service
members should be issued an additional
M291 Skin Decontaminating Kit (fig E-l).
The M291 kit will be carried in the protective mask carrier or as specified in unit
SOP.
c. Orders to start taking the NAPP will be issued
by the proper authority within the chain of command.
d. Resupply will be provided by combat, combat
support, and combat service support units.
2-19. Effects of Pyridostigmine Bromide
a. Pyridostigmine bromide protects an enzyme
(known as acetylcholinesterase) in the body from the
2-16
action of nerve agents. Muscles function as a result
of nerve impulses and the release of specific chemical
substances. A chemical transmitter, acetylcholine,
acts at the neuromuscular junction (where the nerve
interfaces with the muscle) (fig 2-3). When a nerve
impulse reaches the neuromuscular junction, acetylcholine is released, thereby causing the muscle to
contract. The enzyme, acetylcholinesterase, stops the
action of acetylcholine on the muscle after the muscle
has contracted. Nerve agents block the acetylcholinesterase; there is an accumulation of excessive
acetylcholine at the neuromuscular junction resulting
in nerve agent poisoning and its accompanying symptoms. Pyridostigmine protects acetylcholinesterase
against nerve agents, thus preventing the accumulation of excessive acetylcholine when the MARK I is
administrated.
b. Pyridostigmine is not a “true” pretreatment. A
true pretreatment would, by itself, provide some
protection against chemical agents. Pyridostigmine is
an antidote enhancer. Though NOT providing protection by itself, pyridostigmine significantly ENHANCES
the efficacy of the MARK I within 1 to 3 hours after
taking the first tablet. Maximal benefit develops with
time and is reached when a tablet is taken every 8 hours.
FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11
2-20. Principles in the Use of the Nerve
Agent Pyridostigmine Pretreatment
Tablet Set
a. To be maximally effective, one pyridostigmine
bromide tablet should be taken every 8 hours on a
continuous basis prior to exposure to a nerve agent
until all 21 tablets in the blister pack have been taken,
or the individual has been directed to discontinue
taking the medication. If pyridostigmine is to be
continued, another blister pack of the medication must
be issued. This regimen maintains an effective blood
level of the medication. If a tablet is not taken every
8 hours, the beneficial effect of pyridostigmine as a
pretreatment significantly diminishes after 8 hours
from the last tablet.
b. The use of the pyridostigmine pretreatment
medication does not change the administration of
MARK I.
e. The NAPP should not be taken during pregnancy.
NOTE
Do not attempt to give a NAPP tablet to a
casualty with nerve agent symptoms.
2-21. Administration of Pyridostigmine
Pretreatment in an Uncontaminated
Environment
One 30-mg tablet is to be taken by mouth, with
sufficient water to assist in swallowing the medication,
every 8 hours as directed by your commander. If a
dose is missed, do not make it up. Do not take 2
tablets at once because of a missed dose—merely start
again with 1 tablet every 8 hours. Taking 2 tablets at
once could result in adverse side effects. Taking more
than 1 tablet at a time DOES NOT provide additional
protection—in fact, it maybe more hazardous if there
is exposure to a nerve agent.
a. When the order to take pyridostigmine pretreatment has been given, it should be taken as
directed, even though the protective mask is worn.
b. During hours of darkness while in an uncontaminated environment, the NAPP will be administered using the above schedule.
c. At times a commander may have to make a
decision to defer administration of the NAPP on
schedule. Examples of this would be when service
members—
(1) Have experienced sleep deprivation. The
commander would have to decide whether the service
members should be allowed to sleep or be awakened
to take the pretreatment.
(2) Are in a contaminated environment. The
commander would have to decide whether or not to
delay administration of the medication until the unit is
safely out of the contaminated area (para d below). In
any case, the benefits versus the risks should be
carefully weighed before a decision is reached.
d. When the order to take pyridostigmine has been
given, it should be taken as directed (para 2-21). As
long as the environment is contaminated, it is desirable
to continue the pretreatment. The pretreatment should
continue regardless of MOPP level since the protective
posture could be breached at any time. Command
guidelines should be developed for situations such
as—
(1) Providing collective protection or rest and
relief shelters so that personnel can remove their
protective mask and take the tablets, or relocate small
groups to an uncontaminated area, if possible.
(2) Taking the tablets while in MOPP 4 would
be hazardous. (Examples: Troops are operating at
night without lights or are in a chemical agent vapor
environment.) In either case it would be more appropriate to delay taking the medication for a few
hours until the tablets can be taken in a less hazardous
environment.
2-22. Signs and Symptoms of Pyridostigmine Bromide Overdose, Adverse
Reactions, and Contraindications
Although no detrimental effects are expected at the
recommended dosage, depending on the length of time
and the amount of medication taken, as well as
individual physiologic variations, some individuals
may have contraindications for taking pyridostigmine bromide while others may experience adverse
reactions.
a. Signs and symptoms of overdose, adverse reactions, or side effects are—
(1) Abdominal cramps.
(2) Nausea and vomiting.
(3) Diarrhea.
(4) Blurring of vision, miosis.
(5) Increased bronchial secretions.
(6) Cardiac arrhythmias, hypertension.
(7) Weakness, muscle cramps, and muscular
twitching.
(8) Skin rash.
b. Since pyridostigmine bromide may increase
bronchial secretions and aggravate bronchiolar constriction, caution should be used in its administration
to personnel with bronchial asthma.
c. Pyridostigmine bromide may cause urinary
obstruction.
d. Additional contraindications include hyperthyroidism, sensitivity to bromide, peptic ulcer disease,
and low serum acetylcholinesterase.
e. If any of the above signs/symptoms occur, the
service member should consult unit medical personnel
as soon as possible.
2-17
FM 8-285/NAVMED P-5041/AFJMAN 44-149/FMFM 11-11
2-23. Emergency Medical Treatment for
Pyridostigmine Adverse Side Effects,
Allergic Reactions, and Overdose
Ordinarily, discontinuing pyridostigmine should be
adequate to alleviate the signs and symptoms of
adverse side effects, allergic reactions, and overdose.
Pyridostigmine may persist in the blood for as long as
24 hours; however, after the blood level peaks in
about 4 hours, the effects of the medication diminish
gradually.
a. Emergency treatment for an overdose of pyridostigmine requires the administration of atropine in
adequate doses to overcome the cholinergic crisis.
Initially, the 2-mg atropine autoinjector found in the
MARK I kit should be used. In most cases, this will
be sufficient. Further administration of atropine may
be necessary to control the cholinergic effects of
pyridostigmine. If additional atropine is required,
2 mg should be administered by medical personnel
every 15 to 20 minutes, thereby permitting the previous injection of atropine to exert its anticholinergic
effect prior to the next injection.
b. SEVERE cases may require assisted ventilation
because of weakness, but would be unusual when the
pretreatment medication was administered every 8
hours as directed.
c. When stabilized, the patient should be
evacuated for further observation and treatment.
2-24. Responsibilities
a. The corps/division/wing commander will–
(1) Decide whether to begin, continue, or
discontinue the administration of NAPP based on the
threat. The intelligence officer, chemical officer, and
the surgeon act as advisors to the commander in
making his decision if a chemical nerve agent threat
exists (for example, the enemy having nerve agents in
the combat zone or the probability of their use). After
3 days of self-administration of NAPP by the service
member, combat conditions should be reevaluated by
the commander and his staff to determinate whether
to continue the medication or not. However, orders
to discontinue the pretreatment CAN and SHOULD
be made at any time, depending on the situation. If
the pretreatment is to be continued, then a second
blister pack must be ordered while the service member
completes the administration of the 7 days (21 tablets)
and is issued the second pack on the 7th day. Administration of the medication beyond 14 days is not
2-18
recommended without a thorough evaluation of the
situation and recommendation of the medical authority.
However, the magnitude of the threat may outweigh
any possible adverse side effects and indicate continuance of the pretreatment.
(2) Train the service members to faithfully
take the NAPP as directed to enhance their survivability if they are exposed to a nerve agent. Service
members must be trained to take the NAPP during the
day, at night, and while in MOPP 4, should these
procedures become necessary.
(3) Issue unit SOPs for the retention and
decontamination of the NAPP blister pack during
personnel decontamination and overgarment
exchange.
b. Units will–
(1) Obtain the supplies of NAPP through
medical supply channels.
(2) Maintain at least a 2-week supply of NAPP
per member of the unit. One NAPP is issued to each
member of the unit. An additional week’s supply of
NAPP for each individual in the unit will be maintained in the unit area. Authorized quantities will be
commensurate with the latest doctrine for its use.
(3) Store the NAPP for individual issue and
request replacements as the items are issued, or as
they exceed their labeled shelf life. The NAPP should
be stored (refrigerated) in temperatures ranging from
350 to 46°F (2° to 8°C). If the medication is removed
from refrigeration for a total of 6 months, it should be
assumed that it has lost its potency and should not be
used.
(4) Issue the NAPP to the service members
at the time the chemical protective ensemble is
expected to be opened for use.
c. Unit medical personnel will—
(1) Recognize the signs and symptoms of
pyridostigmine overdose, adverse reactions, and side
effects (para 2-22 above) for determining, on an
individual basis, whether or not a service member is
to continue the NAPP based on any adverse reaction
to the medication.
(2) Advise the commander if any serious
problems occur.
d. The individual service member will—
(1) Take the NAPP as directed and in
accordance with the provisions of paragraph 2-20
above.
(2) Secure the NAPP against loss.